Background: 

Implantation of bare metal stents (BMS) induces the release not only of particulate debris, but also of soluble vasomotor substances which contribute to microvascular impairment. We have now addressed the potential attenuation of vasoconstriction by use of paclitaxel eluting stents (PES).

Methods: 

Using a distal protection/aspiration device, coronary arterial blood was retrieved before and during stent (n = 14 BMS, n = 14 PES) implantation in patients with saphenous vein aorto-coronary bypass stenosis and analyzed for vasomotor substances. Vasoconstriction of rat mesenteric arteries with intact (+E) and denuded (-E) endothelium in response to coronary arterial or aspirate plasma was quantified and normalized to that by potassium chloride (KCl_max=100%).

Results: 

Coronary arterial plasma before stent implantation induced a vasoconstriction of 30–43% of KCl_max, which was independent of endothelial integrity. Serotonin-release was 2.2±0.5 mmol/l with BMS and 2.0±0.4 mmol/l with PES, thromboxane B₂-release was 26±5 pg/ml with BMS and 22±8 pg/ml with PES. BMS-aspirate plasma induced a vasoconstriction of 68±18% (+E) or 93±14%(-E), respectively. In contrast, PES-aspirate plasma induced only minor vasoconstriction (+E: 8±3, -E: 12±5% of KCl_max). Addition of paclitaxel to BMS-aspirate plasma also attenuated vasoconstriction. PES-aspirate induced microtubular condensation as seen with immunofluorescence microscopy.

Conclusion: 

Aspirate from PES implantation attenuates vasoconstriction, possibly secondary to microtubular stabilization. Such downstream vascular paralysis could be beneficial in preventing a no-reflow phenomenon in patients undergoing stenting.